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Figure 2 | Breast Cancer Research

Figure 2

From: Endocrinology and hormone therapy in breast cancer: New insight into estrogen receptor-α function and its implication for endocrine therapy resistance in breast cancer

Figure 2

Membrane or nongenomic functions of ER-α. Estrogen (E) or tamoxifen binds membrane or cytoplasmic estrogen receptor (ER)-α to trigger complexes with growth factor signaling molecules (such as insulin-like growth factor [IGF]-R1, insulin receptor substrate [IRS]-1, or phosphatidylinositol-3-OH kinase [PI3K]), which activate mitogen-activated protein kinase (MAPK) or AKT. ER-α also acting as a G-protein-coupled receptor activates Src, which activates matrix metalloproteinase (MMP)-2, which cleaves heparin-binding epidermal growth factor (Hb-EGF) from the membrane to bind and activate EGF receptor (EGFR). EGFR also activates MAPK and AKT, which in turn can phosphorylate and activate nuclear ER-α and amplified in breast cancer (AIB)1, or directly contribute to tumor growth and survival (dotted line).

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